Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
The effects of estradiol (E2) and progesterone on the oxytocin receptor (OTR) were investigated in MCF-7 and Hs 578T human breast cancer cell lines. OTR messenger RNA and protein were identified by reverse transcriptase polymerase chain reaction (PCR) and solution-phase hybridization-RNase protection assay, and Western blot analysis, respectively, in cell lines and in cancerous breast tissue removed from women at mastectomy. Cells were exposed to E2, progesterone, or vehicle (each steroid, 10(-10)-10(-6) M) for 24 h and harvested for extraction of RNA. The OTR PCR product was increased by E2 (10(-7) M, p < 0.05, or 10(-6) M, p < 0.01 vs control) and decreased by progesterone (control vs 10(-7) or 10(-6) M, each p < 0.005). Hs578T cells were cultured in the presence or absence of E2 (10(-6) M) or progesterone (10(-6) M) for 24 h and binding was measured. For the E2-exposed cells, the Kd (p < 0.05), and Bmax (p < 0.01) were higher whereas for the progesterone-treated cells the Kd (p < 0.05) and Bax were lower than control cells. E2 and progesterone not only regulate OTR expression and binding in normal mammary myoepithelium but also in malignant mammary cell lines.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1385/ENDO:18:1:79 | DOI Listing |
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